Frank Horwill

Caution!

These articles were first published many year's ago and whilst some are as relevant today as they were when new, many are now mostly of historical interest as modern research and coaching methods have superseded them.

Twelve Things You Should Know About Your Mitochondria That Could Change the Way you Train

By Frank Horwill

Mitochondrion (singular) and mitochondria (plural), are a sub-cellular structure found in all aerobic cells in which the reaction of the Krebs cycle and electron transport system take place. The Krebs cycle is a series of chemical reactions occurring in mitochondria in which carbon dioxide is produced and hydrogen ions and electrons are removed from carbon atoms (oxidation): also referred to as the tri-carboxcyclic acid cycle (TCA), or citric acid cycle. The mitochondria, which take up oxygen, represent the powerhouse of a cell and are also frequently referred to as the ‘aerobic furnaces’. Here, fuel and oxygen enter into energy-yielding processes resulting in the formation of ATP (Adenosine triphosphate), which is stored in all muscle cells. Only from the energy released by the breakdown of this compound can the cell perform its specialised work.

Mitochondria are invisible to the naked eye and an average microscope; an electron microscope is required. They are sausage-shaped and are just a few micrometres long.

The mitochondrion has two membranes, the inner one forms folded structures (the cristae) extending into the matrix of the structure. Each membrane consists of layers of protein and lipid (fat) molecules. The respiratory chain system is associated with the protein layer. The process of oxidative phosphorylation involves the lipid layers. The enzymes of the Krebs cycle are located in the fluid matrix, the soluble part of the mitochondrial interior.

The more mitochondria an athlete possesses, the better will be endurance performance. This is because they are the only cells where carbohydrates, fats and proteins can be broken down in the presence of oxygen to create energy for exercise.

Interest in the function of mitochondria dates back to the early 1950s, when physiologists observed that the breast and wing muscles of chickens had few mitochondria, while those of pigeons and mallards contained high densities of the minute structures. Because chickens can’t fly, while pigeons and mallards are noted for their endurance feats, this led physiologists to believe that mitochondria concentrations were closely related to aerobic capacity.

A startling discovery was that mitochondria possess their own genetic material and all the mitochondria in an individual’s body are inherited from one’s mother, not father. This is because the egg contains mitochondria, while sperm cells are mitochondria free. This may seem peculiar, since the egg is static and the sperm are endurance swimmers, but the basic fact is that sperm are so minute that mitochondria would be too great a weight for them to bear on their marathon trip to the egg. Contrary to popular belief, exercise capacity is inherited from our mothers, not our fathers. So, if one’s father is a great athlete or a non-active person, it doesn’t really matter, but if one’s mother was a good athlete, it’s a big bonus.

First attempts by physiologists to increase the mitochondrial density were via the endocrine system – and they had some success. Mitochondrial numbers did increase when levels of a key hormone produced by the thyroid gland – thyroxine – increased. Laboratory rats given a supplement of dessicated thyroid in their normal diet responded with a major increase in mitochondrial size and density in both the heart and liver. Thyroxine as an ergogenic aid was very much on the cards for a while, until it was discovered that above average concentrations of this hormone could produce some very unwelcome side effects.

It was the work of physiologist John Holloszy of the Washington University School of Medicine in St Louis, that showed that continual exercise could put mitochondrial numbers on the increase. He induced one group of lab rats to run on a treadmill for up to 2 hours per day at intensities of about 50 to 75 per cent of V02 max or 12 weeks, while a second group rested in their cages. At the end of this exercise, Holloszy found that the running rats had increased their mitocondrial densities by about 50 to 60 per cent and had also doubled their concentrations of ‘cytochrome c’, a key compound found inside mitochondria which is vitally important in aerobic energy production. Cytochorme c contains one atom of iron per mol and is a power-house of amino acids. Holloszy’s work, at first suggested that Van Aaken’s postulations that the best way to gain endurance was by LSD (Long, Slow Distance) were on the right track. Holloszy pressed on with further research. He had one group of rats running 10 minutes per day, another running for 30 minutes, a third group exercising for 60 minutes and a fourth working for 2 hours a day. Training took place five days a week for 13 weeks at an intensity of 1.2 mph, about 32 metres per minute and 313 minutes for the 10K, which is about 50-60 per cent VO2 max for a fit lab rat. As expected, the 2 hours per day runners had the best mitochondrial development. The 10 minute per day exercisers had about 16 per cent more cytochrome c than the resting group of rats, while the 30 minute ones boosted it by 31 per cent, the one hour runners by 38 per cent and the 2 hour runners increased it by 92 per cent. These findings in 1967 were a potent argument for "Run long, run slow, run gently". Holloszy’s work was given more credence when in a run to exhaustion test, the 2 hour trainers kept going at a good pace for 111 minutes, while the 10 minute trainers lasted 22 minutes, the 30 minute ones for 41 minutes, the one hour rats ran strenuously for 50 minutes. The relationship of a high cytochrome c level to better performance had been firmly established.

Holloszy’s research was heralded by Lydiard fans with glee. He advocated building up to 100 miles a week of slow running for 10 consecutive weeks in the winter. Some runners, such as Dave Bedford, took the mileage quota as far as 200 miles a week done in three sessions a day. However, Holloszy’s work, good as it was, had a flaw – it did not work at training intensity as a mitochondrial development factor – all his rats ran at the same speed.

In 1982, Gary Dudley, at the State University of New York at Syracuse, investigated the effect of intensity on mitochondrial production. His work was painstaking – rats were made to run five times a week for periods ranging from five minutes to ninety minutes per day, for eight weeks (five weeks less than Holloszy’s rats), at training intensities which ranged from 40 per cent through to 100 per cent V02 max. Dudley also examined how different speeds and durations influenced different muscle fibres (fast twitch, aerobic fast twitch or intermediate and slow twitch), which no one had ever done before. His findings were as follows:

Training beyond about 60 minutes per workout was without benefit in terms in increasing cytochrome c. Moving from 30 minutes to 60 minutes per session did increase cytochrome c, but not increasing the workout from 60 to 90 minutes. This was true of all intensities studied by Dudley – and also with all three muscle fibre types. Mitochondrial development ceased after an hour.

Training for 10 minutes a day at 100 per cent of the V02 max (about 3K pace) tripled cytochorme c concentration.

Running for 27 minutes at 85 per cent V02 max (about 10 seconds per mile slower than 10k speed), only pushed up cytochrome c by 80 per cent.

Training at 60 to 90 minutes at 70 to 75 per cent V02 max (marathon speed), edged up cytochrome c by just 74 per cent.

In intermediate muscle cells (those which are roughly half way between fast twitch and slow twitch), a similar potency of intensity was recorded. Ten minutes of fast running per day boosted cytochrome c as much as 27 minutes daily at 85 per cent V02 max or 60 to 90 minutes at 70 to 75 per cent V02 max.

The best strategy for slow-twitch, cytochrome c enhancement was running for 60 minutes per outing at 70 to 75 per cent V02 max (around 80 to 84 per cent of maximal heart rate), which boosted cytochrome c by 40 per cent.

Cruising along for 27 minutes at 85 per cent V02 max produced a 28 per cent upturn as described above.

Fast running at 100 per cent V02 max (3K speed), lifted slow twitch cytochrome c by around 10 per cent, not a surprising low gain because slow twitch muscles are less heavily used than fast twitch cells during fast running. However, running at this speed represents, for 10 minutes work, 1 per cent improvement per minute of running compared to running at 85 per cent V02 max, which lifted cytochrome c in slow-twitch fibres by the same 1 per cent per minute rate for nearly three times the duration of work. And, further, 90 minutes of 70 to 75 per cent V02 max work improved the mitochondria by just two-thirds of a per cent per minute.

Dudley et al. sum up, "To bring about the greatest adaptive response in mitochondria, the length of daily exercise becomes less as the intensity of the exercise is increased."

The author in 1950 decided to run 2 miles full out every other day for a month. On other days, he ran 6 miles slowly. Two mile pace equates to 3,000m speed (100 per cent V02 max). He then ran the penultimate 4 mile leg of the Portsmouth to Southampton relay and broke the course record. He did not, of course, know of Dudley’s findings, but in retrospect, it would appear that the training at 100 per cent V02 max caused a major fitness improvement. The bottom line is that either running 5K or 3K each week at maximum effort is going to boost the mitochondria, which, of course, will improve the V02 max. Alternatively, sections of those distances can be run at slightly faster than race pace.
5K pace sessions include:

3 x 2000m with 2 mins rest

4 x 1 mile (1,609m) with 90 secs rest

6 x 1,000m with 60 secs rest.

Useful 3 pace sessions include:

3 x 1,500m with 3 mins rest

6 x 800m with 90 secs rest

16 x 400m with 45 secs rest

Note that if the 5K pace session is run at 80secs/400m, the 3k pace session should be 4-5 seconds faster, i.e. in this case 75-76secs/400m. Note that Britain’s greatest ever middle distance runner, Seb Coe (12 world records in 4 years, Olympic gold and silver medals), trained at 5K speed weekly throughout the winter and at 5K and 3K speed throughout the track season. The former being 95 per cent of the V02 max.